Apolipoprotein AV, the guide of chylomicron and regulation of TAG fate in adipose tissue

Lipogenesis and lipolysis are two enzyme reaction that related to each other like two sides of coin. This process make sure that we have enough energy when the source of food is depleted. Our body automatically store excess fat and carbohidrate into lipid in the form of triacylglycerol or TG. Adipose tissue and liver are two major site where this process take place.

After meal and digestion already done by our gastrointestinal track, fat that come from food is circulated in blood inside a droplet called chylomicron or in the form of lipoprotein. This molecule basically is a lipoprotein with protein at the outer later to make sure that hydrophobic material inside could be transported via hydrophilic environtment. And the major source of TAG in white adipose tissue (WAT) is circulating in VLDL or very low density liporotein. However, in order to be taken by adipose tissue, this molecule should shifted into different form because the size is to big for penetration through endothelial cells. That is why lipolysis in this process is essential because the huge molecules will be broken down into small molecules and can be transferred into adipose tissue.

The breakdown of the huge molecule (TAG) into small molecule (fatty acid) happends in endothelial cells. This process is done by enzymatic activity of lipoprotein lipase or LPL. LPL secreted by adipose tissue into endothelial cells thus bind to its substrate, TG. TG is broken down into non-esterified fatty acid or NEFA. NEFA then could be taken by adipose tissue and then changed again into TAG for storage. Some NEFA could escape to the circulation via albumin.

Recent study shown that ApoAV might play an important role in the regulation of TAG uptake by adipose tissue. It has been shown that ApoAV could guide VLDL and chylomicron to LPL so lipolysis can be done. This process is still poorly understood and its not widely known how TAG rich lipoprotein is delivered into LPL. However, study in human shown that SNPs across ApoAV locus is related to plasma TAG level. Studies in animal model using knock out mice of ApoAV showing that impresent of this protein would lead to increase TAG. Its been predicted that this effect is due to inability of LPL to react with TAG rich lipoprotein.